December 29, 2012

The researchers assessed development of pain-related behaviors and concomitant changes in dorsal root ganglia (DRG), nerves that carry signals from sensory organs toward the brain. They found that a chemokine known as monocyte chemoattractant protein (MCP)-1 (CCL2) and its receptor, chemokine receptor 2 (CCR2), are central to the development of pain associated with knee OA. . . .

Mice that lack Ccr2 (knockout mice) also developed mechanical allodynia, but this began to resolve from eight weeks onward. Despite having severe allodynia and structural knee joint damage equal to that in normal mice, Ccr2-knockout mice did not develop movement-provoked pain behaviors at eight weeks.

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